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dc.creatorRoganovic, J.
dc.creatorDjukic, L. J.
dc.creatorKrsljak, E.
dc.creatorTanic, N.
dc.creatorStojic, D.
dc.date.accessioned2016-05-23T10:59:43Z
dc.date.issued2015
dc.identifier.issn1601-0825
dc.identifier.urihttps://ibiss-r.rcub.bg.ac.rs/handle/123456789/1939
dc.description.abstractObjectivesThe influence of experimental diabetes (alloxan, 100mgkg(-1)) was studied on rabbit parotid gland function. Material and MethodsCarbachol-induced parotid secretion in vivo, and in vitro quantification of inducible nitric oxide synthase (iNOS) mRNA expression, by real-time RT-PCR, and activity of superoxide dismutase (SOD) and total antioxidant capacity (TAC) in commercial colorimetric assays were measured in parotid glands of non-diabetic and diabetic rabbits. ResultsCarbachol-induced dose-dependent increase in parotid secretion significantly reduced in diabetic rabbits. Functional studies in the presence of muscarinic receptor and nitric oxide synthase (NOS) antagonists revealed that in M-3 receptor-mediated carbachol secretion, nitric oxide, deriving mainly from neuronal NOS (nNOS) in control, and iNOS in diabetic rabbits, was involved. Also, upregulation of iNOS mRNA expression and enhanced SOD activity and TAC were detected in diabetic glands. ConclusionsOur data suggest that decreased M-3 receptor-mediated parotid secretion in diabetic rabbits appears to be due to alterations in NO signaling, mainly due to iNOS induction, accompanied by elevated antioxidant response.
dc.description.sponsorshipMinistry of Science and Technological Development, Serbia-Research Grant {[}175021]
dc.languageEnglish
dc.rightsrestrictedAccess
dc.sourceOral Diseases
dc.subjectdiabetes
dc.subjectparotid secretion
dc.subjectinducible nitric oxide synthase
dc.subjectoxidative stress
dc.titleReduced muscarinic parotid secretion is underlain by impaired NO signaling in diabetic rabbits
dc.typearticle
dc.rights.licenseARR
dcterms.abstractТаниц, Н.; Дјукиц, Л. Ј.; Рогановиц, Ј.; Крсљак, Е.; Стојиц, Д.;
dc.citation.issue5
dc.citation.volume21
dc.identifier.doi10.1111/odi.12327
dc.identifier.scopus2-s2.0-84930276185
dc.identifier.wos000355741700012
dc.citation.spage634
dc.citation.epage640
dc.type.versionpublishedVersionen


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